It is the long range purpose of this project to study the control mechanisms important in regulating cell growth, neoplastic transformation, and protein synthesis in normal and malignant cells of the immune system. To this end we are studying the structure of the proto-oncogenes in normal and tumor tissues from mouse and man and the expression of these oncogenes as mRNAs. In particular we are focusing on mouse plasmacytomas, myelogenous tumors and lymphosarcomas, and we investigating what role Abelson and Moloney leukemia viruses play in the induction of such tumors and the alteration of cellular ongogenes. We have discovered that these viruses induce a morphologically distinct subset of tumors (ABPLs) which have altered myb mRNAs owing to the insertion of a deleted form of Moloney leukemia virus in the myb gene. This represents a mammalian example of oncogene activation by promoter/enhancer insertion of virus. The ABPL tumors now appear to be of myelogenous origin, so we are studying the myb genes in other mouse myelogenous tumors. The expression of c-myc is increased in plasmacytomas, and in certain plasmacytomas with chromosomal translocations just 5' of the myc exon I, RNA transcription utilizes the two myc promoters in a different ratio than in normal cells. Two of these plasmacytomas are super producers of myc RNA and are being studied for clues to the mechanism of this enhanced RNA synthesis. We are also studying the expression of oncogens in mouse and human autoimmune diseases, as well as their expression of oncogenes in mouse and human autoimmune diseases, as well as their expression in normal lymphocytes activated by mitogens. Certain classes of autoimmune diseases are characterized by high levels of myc and raf RNA, while others have elevated levels of myb RNA.